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Alzheimer's disease (AD) elevates extrasynaptic GluN2B (ES-GluN2B) and decreases polysialylated neural cell adhesion molecule (PSA-NCAM) in the brain. Amyloid-beta (Aβ) may drive these changes by downregulating PSA-NCAM synthesis enzymes, suggesting therapeutic targets for AD.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Neurodegenerative Diseases

Background:

  • N-methyl-D-aspartate receptors (NMDARs), particularly GluN2B subunits, are crucial for synaptic plasticity.
  • Extrasynaptic GluN2B (ES-GluN2B) activation is implicated in long-term depression and potentially Alzheimer's disease (AD) dementia.
  • Polysialylation of neural cell adhesion molecule (NCAM) to PSA-NCAM, regulated by ST8Sia4 and UDP-E, normally inhibits ES-GluN2B activity.

Purpose of the Study:

  • To investigate the spatiotemporal dynamics of ES-GluN2B and PSA-NCAM in aging and AD.
  • To determine the effects of amyloid-beta (Aβ) on these proteins and their regulatory enzymes.

Main Methods:

  • Examined NMDAR subunits, ES-GluN2Bs, NCAM, and PSA-NCAM expression in young/old Tg2576 AD mice and wild-type (WT) controls.
  • Utilized immunoblotting and pull-down assays across brain regions.
  • Assessed Aβ's neurochemical effects on ST8Sia4, PSA-NCAM, and UDP-E in IMR-32 neuroblastoma cells via protein and mRNA quantification.

Main Results:

  • Aging reduced GluN2B and increased GluN2A expression. AD mice showed elevated ES-GluN2B and downregulated PSA-NCAM, especially in the hippocampus and prefrontal cortex.
  • Normal aging increased PSA-NCAM expression.
  • Aβ treatment significantly downregulated ST8Sia4, PSA-NCAM, and UDP-E expression and mRNA levels in neuroblastoma cells.

Conclusions:

  • AD is characterized by increased ES-GluN2B and decreased PSA-NCAM, distinct from normal aging.
  • Aβ may induce these changes by downregulating ST8Sia4 and UDP-E, linking Aβ activity to PSA-NCAM dysregulation in AD.
  • These findings highlight potential therapeutic targets for AD intervention.